UF undergrad and surgery lab researcher named to University Scholars Program
Catherine Miney, a senior biomedical engineering major at UF, was recently accepted into the University of Florida (UF) University Scholars Program. She is currently a student in a lab overseen by UF Department of Surgery faculty.
Miney’s work focuses on understanding the role a certain protein plays in blocking cellular destruction in patients with chronic non-alcoholic fatty liver disease (NALFD).
She is working under the guidance of Jae-Sung Kim, Ph.D., an associate professor in the department of surgery, pharmacology and therapeutics, the Institute on Aging, and anatomy and cell biology. Students in the program take on a full research project under the guidance of a faculty member. Miney’s project begins this summer and completes next spring.
“The University Scholars Program is a great opportunity to foster young undergrads as potential scientific investigators. The selection criteria are very strict,” Kim said. “Catherine is incredibly smart, and she has an outstanding work ethic. She also grasps new ideas very quickly. Catherine is able to read and understand science papers that are usually geared toward graduate students and professionals.”
The causes of NAFLD remain largely unknown. People who have the condition are most likely middle-aged and overweight, and they also tend to have diabetes and high cholesterol.
The researchers believe that chronic NAFLD is linked autophagy dysfunction — a process where the body releases proteins that target excess fat deposit and defective or damaged parts of a cell called mitochondria. Miney and her team believe that enhancing the production of a certain protein can facilitate liver cells to remove excess fat and to clear dysfunctional mitochondria.
While mitochondrial dysfunction is linked to NAFLD, scientists do not yet know the exact role mitochondria plays in the disease, Miney said. Most studies have focused on ways the mitochondria process high amounts of fat.
In a mouse model, researchers are treating liver cells with palmitic acid to replicate the effects of NAFLD and analyzing changes in certain proteins over 24 hours. Specifically, the team is targeting the chronic form of the disease.
“So far, over time, we’ve seen changes in autophagy in the mouse cells treated with palmitic acid. Cells that are not treated with palmitic acid seem to sustain a steady autophagy,” Miney said. “We are trying to figure out why that is happening.”
Miney found that fat intake to the liver affects mitochondria, and too much fat intake significantly changes the mitochondrial autophagy — or mitophagy — process, Kim said. The changes aren’t immediately after fat intake — it takes time.
“We believe mitochondrial autophagy is an important process to handle fat uptake,” Kim said. “We always thought that mitochondrial autophagy took effect immediately. Surprisingly, we found that it takes some time.”
Miney’s data suggest that one-time or occasional exposure to a high-fat diet “is not that detrimental to the mitochondria” or may not place a person at a higher risk for NAFLD, Kim noted. “Repeated or chronic exposure makes the mitochondria dysfunctional or defective.”
The long-term goal, Kim said, is to develop therapeutic strategies against NAFLD and its progression to liver cirrhosis and cancer.